Over 90% of peanut allergic children react on their first known exposure. The route by which sensitisation occurs is unclear. Much work has focused on maternal consumption of allergen (during pregnancy or lactation) yet interventional studies have failed to demonstrate any benefit of dietary elimination. Recent data demonstrate that rashes and the topical application of peanut-oil containing preparations to the infant’s skin are risk factors for the development of peanut allergy. This suggests that this low dose cutaneous exposure is a likely route of sensitization. However, consumption of peanut containing foods by household members, especially during the child’s first year of life, is another important source of environmental peanut exposure.

Our study aimed to investigate the role of the infants’ environmental peanut exposure in the later development of allergy. We designed a dietary questionnaire to retrospectively measure an individual’s weekly peanut consumption. This was used in a cohort of children with peanut allergy and age-matched controls. We thus quantified peanut consumption by all household members during infancy as well as maternal peanut consumption during pregnancy and lactation. Details of numerous other possible risk factors for peanut allergy were also collected. Recall bias regarding peanut consumption by families whose child was known to be peanut allergic was avoided by obtaining data before such a diagnosis was suspected. This required administration of the questionnaire to children with difficult eczema or other food allergies who had not reacted to peanuts in the past. After information on peanut consumption had been obtained, the data was only utilised if later allergy testing to peanut returned values that were >95% positive predictive values for clinical allergy. Two groups of controls were recruited. A High Risk Control group included children with proven egg allergy (have a 30-50% chance of having peanut allergy) but who were not sensitised to peanut. A further group of Normal controls comprised of children attending General Paediatric Clinics with a non allergy related problem.

Median weekly household peanut consumption during the first year of life in the peanut allergic Cases (n=133) was 78.9g as compared with 29.1g in the Normal controls (n=150) and only 7.8g in the High Risk Controls (n=160). Pair-wise comparisons between the three groups each gave significant differences with a p-value <0.0001. Similar effects were noted when consumption was considered in terms of episodes of peanut consumption or only peanut butter consumption. Differences in maternal peanut consumption during pregnancy and lactation were less significant and become nonsignificant after adjusting for other dietary factors. The form that peanut was consumed in also appeared to be important, with peanut butter consumption leading to the greatest risk of peanut allergy.

Some infants in the high risk control group, who were not peanut sensitised, were found to have high peanut consuming households. However, these infants differed from other High Risk controls, in that they were significantly more likely to have consumed peanut themselves. This highlights the critical T07043 4 Final Technical Report importance of the route by which allergen exposure occurs and implies that early oral exposure may induce tolerance, thus protecting children from potential sensitisation by low dose environmental exposure.

We also investigated the awareness and uptake of Department of Health Guidance aimed at preventing peanut allergy. We found that a combination of lack of awareness, misunderstanding of their relevance, lack of will or difficulty in following the DoH guidance has resulted in only 17% of the target mothers successfully adhering to it. However, the greater proportion of mothers adhering to the advice in the High Risk controls, relative to the peanut allergic Cases (p=0.025), suggests that the guidance did have some efficacy in preventing peanut allergy. However, this may not be due to the mechanistic theories upon which the advice was based.

Investigation of a number of other possible risk factors for peanut allergy failed to reveal any other specific influences. This included the application of peanut or soya containing creams, which were not found to be a specific risk factor for peanut allergy, although a marked decrease in the level of usage of peanut containing creams is the most likely explanation for our failure to replicate previous findings.

Comparison of all the food allergic children to non food allergic controls revealed higher rates of eczema, asthma, wheeze, use of soya milk, family history of atopy and mixed ethnicity amongst the food allergic group but a lower proportion of Caucasians, prematurity and dog ownership.

In conclusion, these results suggest that in susceptible individuals, increased exposure to environmental peanut promotes allergy whilst low levels may be protective. This supports our hypothesis that peanut sensitization occurs as a result of environmental exposure through cutaneous or inhalational routes rather than from maternal or infant allergen consumption. Our data also raise the possibility of early oral exposure playing an important role in the development of tolerance. If sensitization is indeed occurring through environmental exposure, this has important implications for public health policy. Future strategies to prevent allergy might include measures to reduce the levels of environmental peanut in the infant’s milieu or the introduction of peanut orally in early infancy to induce tolerance. Both of these approaches need careful assessment in prospective studies before they could be recommended.